EditorialAtherosclerosis and Autoimmunity

Francesca Romana Spinelli ,1 Francesca Barone,2 Fabio Cacciapaglia,3 Arbi Pecani,4

and Matteo Piga 5

1Sapienza Università di Roma, Rome, Italy2University of Birmingham, Birmingham, UK3Azienda Ospedaliera Policlinico di Bari, Bari, Italy4University Hospital Center “Shefqet Ndroqi”, Tirana, Albania5Università di Cagliari, Cagliari, Italy

Correspondence should be addressed to Francesca Romana Spinelli; francescaromana.spinelli@uniroma1.it

Received 31 December 2017; Accepted 1 January 2018; Published 29 March 2018

Copyright © 2018 Francesca Romana Spinelli et al. This is an open access article distributed under the Creative CommonsAttribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original workis properly cited.

This special issue brings together original research andreview articles focusing on the contribution of innate andadaptive immune response in the endothelial dysfunctionand in the progression of atherosclerosis in autoimmunerheumatic diseases (AIRDs). By pointing out the relationshipbetween immune response and atherosclerosis, it opens awindow of opportunity for therapeutic intervention in themanagement of cardiovascular comorbidity.

AIRDs have been linked to a high risk of cardiovascular(CV) morbidity and mortality, mainly due to prematureatherosclerosis (ATS). Recently, more attention has beenattributed to ATS as an inflammatory, immune-mediateddisease leading to premature vascular damage; mountingevidence supports an independent role for both humoraland cellular immune response, together with the involve-ment of innate immunity, in the development of the athero-sclerotic plaque [1]. The immune system contributes mainlyto endothelial dysfunction (ED), the earliest and reversiblestage of ATS [2]. Recent evidence supports the presenceof premature, accelerated ATS in AIRD patients that cannotbe fully explained by the traditional cardiovascular riskfactors. In this special issue, Z. Wang et al. reviewed theemerging role of the interplay between cigarette smokingand adipose tissue in the progression of atheroscleroticplaque, describing how the exposure to chemicals affectsthe status and functions of adipocytes.

Rheumatoid arthritis (RA) and ATS share manycommon mechanisms responsible for local and systemicinflammation [3]. In their original paper, G. L. Erre et al.evaluated the microvascular endothelial response in a largecohort of RA patients without any previous CV event anddetected peripheral microvascular ED in one-third of thepatients, which was only partially related to traditionalcardiovascular risk factors. In their review of the literature,M. Di Franco et al. addressed the methylarginine metabolismin RA patients; in particular, the authors focused on asym-metric dimethyl-arginine (ADMA) and its implication inthe accelerated atherosclerosis both as a surrogate biomarkerof ED and as a possible target of treatment.

Immune-mediated mechanisms seem to interplay andconverge into a proinflammatory and proatherogenic pheno-type. In this regard, Y. Jeng et al. explored how the abundanceof CD16+ monocyte subset predicts mortality: in a longitu-dinal cohort study, the authors showed that higher numberof CD16+ monocytes correlates with increased mortality(overall mortality and CV deaths) in hemodialysis patients,shedding light on early recognition of immune dysfunctionin this context.

The metabolic effects linking atherosclerosis, autoim-munity, and chronic inflammation are intriguing and stillnot well explored [4]. S. Gao et al. created a transgenic rab-bit model that successfully expressed liver-specific human

HindawiMediators of InflammationVolume 2018, Article ID 6730421, 2 pageshttps://doi.org/10.1155/2018/6730421

cholesteryl ester transfer protein (hCETP) with the abilityto enhance macrophage-derived foam cell formation andincreasing HDL cholesterol and triglyceride plasmatic levels;the authors reported an atherogenic effect of increased CETPactivity during cholesterol-fed diet, supporting a role forCETP inhibition as a cardioprotective intervention. In thelight of these results, the immune system interference withCETP activity should be evaluated in human clinical trialsand considered for therapeutic strategies.

Through this special issue, we also provide new scientificevidence on the potential effects that medications used totreat AIRDs may have on the endothelial function andprogression of atherosclerosis. In vitro experiments from K.Lakota et al. showed that both methotrexate and fluvastatinare highly effective in lowering proatherogenic cytokines.Such an evidence may partly explain the protective effect ofmethotrexate and hydroxychloroquine against acceleratedATS in patients with RA and systemic lupus erythematosusas reviewed by A. A. Mangoni et al. and by A. Floris et al.,respectively. Moreover, the effects of methotrexate andTNF-inhibitors on ADMA serum levels are reviewed in thepaper by M. Di Franco and colleagues.

In this special issue, we emphasized some importanttopics concerning the contribution of the immune systemin the development of ATS in AIRDs, thus shedding lightnot only on the understanding of these mechanisms but alsoon their practical implications.

Francesca Romana SpinelliFrancesca Barone

Fabio CacciapagliaArbi PecaniMatteo Piga

References

[1] P. Libby, “Inflammation in atherosclerosis,” Arteriosclerosis,Thrombosis, and Vascular Biology, vol. 32, no. 9, pp. 2045–2051, 2012.

[2] X. Yang, Y. Chang, and W. Wei, “Endothelial dysfunction andinflammation: immunity in rheumatoid arthritis,” Mediatorsof Inflammation, vol. 2016, Article ID 6813016, 9 pages, 2016.

[3] S. Skeoch and I. N. Bruce, “Atherosclerosis in rheumatoidarthritis: is it all about inflammation?,” Nature ReviewsRheumatology, vol. 11, no. 7, pp. 390–400, 2015.

[4] T. Gaber, C. Strehl, and F. Buttgereit, “Metabolic regulation ofinflammation,” Nature Reviews Rheumatology, vol. 13, no. 5,pp. 267–279, 2017.

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